ArticleFrontiers in immunology2023
Heat shock protein 90 inhibition attenuates inflammation in models of atopic dermatitis: a novel mechanism of action.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- RGRN-305, a novel Hsp90 inhibitor: a promising therapeutic option for inflammatory dermatologic diseases.Inflammopharmacology · 2026Review
- Relationship between hair cortisol and plasma heat shock proteins in response to heat stress in tolerant and sensitive cattle breeds.Scientific reports · 2026Article
- Hsp90 inhibitor 17-AAG reduces skin inflammation and inhibits NF-κB/NLRP3 inflammasome activation in DNCB-induced mice and TNF-α/IFN-γ-induced keratinocytes.Open life sciences · 2026Article
- Quercetin as a Novel Antidepressant: Mechanistic Insights into Its Neuroprotective and Anti-inflammatory Effects.Molecular neurobiology · 2025Article
- NMFProfiler: a multi-omics integration method for samples stratified in groups.Bioinformatics (Oxford, England) · 2025Article
- Hsp90 as a pathophysiological factor and emerging therapeutic target in atopic dermatitis.Frontiers in immunology · 2025Review
- From stress signals to fertility challenges: the role of damage-associated molecular patterns in male reproduction.Frontiers in immunology · 2025Review
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Heat shock protein 90 (HSP90) is an important chaperone supporting the function of many proinflammatory client proteins. Recent studies indicate HSP90 inhibition may be a novel mechanism of action for inflammatory skin diseases; however, this has not been explored in atopic dermatitis (AD). Objectives: Our study aimed to investigate HSP90 as a novel target to treat AD. Methods: Experimental models of AD were used including primary human keratinocytes stimulated with cytokines (TNF/IFNγ or TNF/IL-4) and a mouse model established by MC903 applications. Results: In primary human keratinocytes using RT-qPCR, the HSP90 inhibitor RGRN-305 strongly suppressed the gene expression of Th1- ( Conclusion: HSP90 inhibition by RGRN-305 robustly suppressed inflammation in experimental models mimicking AD, proving that HSP90 inhibition may be a novel mechanism of action in treating AD.
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Registered trials
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